Atherosclerosis is a common progressive disease that occurs when the inside of arteries has plaque buildup. It progresses in stages and may not show any symptoms until the plaque ultimately occludes the arterial lumen or may get dislodged to form a thromboembolic clot.
The consequences of this can be life-threatening if corrective measures are not taken on detection. This is because it limits or stops blood flow and oxygen to the organ of supply, which can be the heart, brain, or kidneys. A heart attack or a stroke is then imminent.
There are several stages of atherosclerosis. Each stage involves specific changes in your artery wall. These changes, though minuscule, ultimately cause serious damage to your artery.
The stages of atherosclerosis progress over many years. They are mostly undetected until symptoms and complications set in.
Stages of atherosclerosis
Atherosclerosis usually starts to develop in the teenage years and 20s. In the early stages, the cardiac evaluation screening tests, such as serum cholesterol may come back normal. By the 30s atherosclerotic changes are seen in most people.
Signs of atherosclerosis mostly begin to appear in men after the age of 45 years and in women after the age of 55 years. This is how atherosclerosis develops over time in stages.
Stage 1: Damage to endothelium and immune response
Atherosclerosis begins to develop when the inner layer of the arterial wall, the tunica intima, gets damaged. The inner surface of the intima, called the endothelium, is lined with endothelial cells. It is intima that stands between the blood and your artery wall.
The most common risk factors that can damage intima include:
- High levels of LDL cholesterol in the blood
- Toxins present in cigarette smoke
- Persistent high blood pressure
Several things happen after the damage to the intima:
Cholesterol from your blood starts adhering to the site of injury. This cholesterol undergoes oxidation to form oxidized cholesterol. This triggers an immune response, which causes white blood cells to surround the cholesterol and form clumps at the injured site on the arterial wall and cause inflammation within the artery.
Stage 2: Fatty streak
A “fatty streak” is a yellow streak made up of dead cells that develop at the site of endothelial damage. It is the first visible sign of atherosclerosis. Here’s how it forms:
- The monocytes, which are white blood cells, called macrophages surround the cholesterol that has adhered to the site of the injured arterial wall.
- As this process develops, the macrophages fill up with cholesterol, take on a foamy appearance, and are then called “foam cells”, which soon die.
- As the foam cells die, more and more white blood cells accumulate at the site, continue to surround cholesterol, become foamy and die. As this process continues, more of the endothelium gets damaged.
- The dead foam cells form a swelling underneath the endothelium. This is the beginning of plaque formation.
Stage 3: Plaque growth
More dead foam cells and other substances continue building up at the site of the fatty streak to form a larger piece of plaque. The plaque is made up of deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin. As it builds up, the arterial walls become thickened, stiff, and lose their elasticity.
The smooth muscle cells of the arterial wall cover and form a layer on top of this plaque called the fibrous cap. It prevents the plaque from breaking off and getting dislodged into the bloodstream. The plaque keeps growing and becomes hard due to its calcium content.
As the plaque grows too big, the lumen of the artery becomes narrower resulting in less space for the blood to flow through. The arterial wall elasticity is exhausted and ultimately the plaque may rupture and get dislodged.
Stage 4: Plaque rupture
In this last stage of atherosclerosis, the plaque ruptures and is exposed to the blood. This can trigger the formation of a blood clot or a thrombus. This blood clot occludes the arterial lumen and blocks the blood flow. The combination of the ruptured plaque with the blood clot is called a complicated lesion.
The plaque has been thus developing in the artery for a long time — perhaps many years. It has gradually grown in size and has been slowly and progressively occluding its lumen. The fibrous cap has kept the plaque in place and prevented it from breaking open until this point.
A thin fibrous cap is more likely to rupture than a thicker one. The size of the plaque may not matter as much because sometimes, a smaller plaque leads to a heart attack.
How fast does atherosclerosis progress?
Atherosclerosis is a slow, progressive disease that may start as early as childhood. However, it can progress rapidly.
Although atherosclerosis is a progressive disease spreading over many years, it is now increasingly noted to progress over a few months to 2 or 3 years in some patients without the usual risk factors. In such cases, the term rapid progression of atherosclerosis is now used.
A study has found that fatty atherosclerotic plaques rapidly build up in people between the ages of 40 and 50 years in the arteries that supply the heart, brain, and legs with blood.
Medical treatment, a disciplined lifestyle of regular exercise, dietary correction, staying at a healthy weight, and vice-free habits can prevent atherosclerosis from progressing and can stabilize the atherosclerotic plaque. However, though they can prevent new plaques from forming, existing atherosclerosis cannot be cured or reversed.